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The Role of Calcium-Activated Pathways in Respiratory Neurons
Maria C. Quintero1, Juan M. Cordovez1 and Robert Putnam2
1Los Andes University 2Wright State University

The cellular factors that determine the magnitude of the firing rate response of respiratory neurons to increased CO2 are typically attributed to acid-induced increased firing rate pathways. Although these activating pathways seem to explain the increased firing rate of chemosensitive neurons in many regions of the brainstem, a marked reduction in the firing rate response to hypercapnic acidosis (HA) has been observed in chemosensitive neurons from the locus coeruleus (LC) during postnatal development [1]. This limited response has been hypothesized to be due to the development of a decelerating pathway that arises from CO2/H+ activation of Ca2+ and Ca2+-activated K+ channels. Although this braking pathway may play an important role in setting the magnitude of the response to increased levels of CO2/H+ in LC neurons, limited attention has been paid to a braking pathway as a candidate mechanism exerting the observed limiting effect in central chemosensitivity [2]. In this work, a single-cell model was employed to simulate the chemosensitive behavior of LC neurons and investigate the effect of a putative limiting pathway driven by CO2 activated calcium currents and Ca+ activated K+ channels. The results from the model support the hypothesis that a calcium-activated braking pathway is responsible for the limited chemosensitivity of LC neurons.

[1] R. W. Putnam, J. A. Filosa, and N.A. Ritucci Am J Physiol Cell Physiol. 287:C1493-C1526 (2004).
[2] M Chernov, J. A. Daubenspeck, J. S. Denton, J. R. Pfeiffer, R. W. Putnam Am J Physiol Cell Physiol. 15:C278-C291 (2007).